CHAPTER 22 Renal Disorders 541
Epstein–Barr virus, hepatitis B or C, or cytomegalo- virus. Autoimmune and immunological diseases such as systemic lupus erythematosus (SLE) frequently cause AGN. Glomerulonephritis can also occur as part of an active infectious process. This type of AGN includes staphylococcus-associated glomeru- lonephritis (SAGN) that develops in people with an infection with methicillin-sensitive or methicillin- resistant Staphylococcus aureus. It can also occur in persons with bacterial endocarditis and central venous catheter infections. AGN of any type can progress to chronic disease, particularly in patients with other risk factors. The course of chronic glomerulonephritis is often grad- ual and silent. By the time of diagnosis, the patient is commonly already in the early stages of ESRD. Pathophysiology Postinfectious glomerulonephritis, the most common type of AGN, begins with an antigen–antibody reac- tion. An antigen, such as streptococcus, enters the body and stimulates antibody synthesis. There are two theoretical explanations for the mechanism of disease. One theory claims that the antibodies attack the antigen, but also form antigen–antibody com- plexes that float freely in the bloodstream until they deposit within glomerular membranes. The other the- ory asserts that molecular mimicry occurs, where the antibodies that are stimulated attack the antigen and mistakenly attack the glomerular membranes as well (see Fig. 22-7).
Continuous Renal Replacement Therapy Continuous renal replacement therapy (CRRT) is similar to hemodialysis; however, it is a slower process used for patients who are hemodynamically unstable and fluid overloaded. This continuous process takes smaller volumes of blood from the patient and filters it through a dialyzer over 24 hours. It is most commonly used in patients with acute kidney injury. Pathophysiology of Selected Disorders Major pathophysiological conditions of the kidney include acute glomerulonephritis, nephrotic syndrome, nephrolithiasis, pyelonephritis, polycystic kidney dis- ease, Goodpasture’s syndrome, acute kidney injury, and chronic kidney disease. Acute Glomerulonephritis Acute glomerulonephritis (AGN) is a renal disorder that is due to inflammation of the glomerulus. In most cases, AGN is due to an immunological mechanism that triggers inflammation that damages the mem- branes of the glomerulus. It can lead to significant illness because the glomerulus is the critical, initial region of every nephron unit that filters the blood. Damage to the glomerular capillaries causes a loss of vital substances, such as albumin, from the blood into the tubule fluid, which becomes urine. Glomerular injury increases glomerular permeability, which allows albumin to leave the capillaries and enter the tubules. Epidemiology Glomerulonephritis may be an acute, mild disease or a rapidly progressive disease that can lead to renal dys- function. AGN is the cause of 25% to 30% of all cases of ESRD. In cases that progress to ESRD, the disease course is fairly rapid. In severe disease, end-stage renal failure may occur within weeks or months of the onset of AGN. Most cases of AGN occur in patients aged 5 to 15 years; only 10% occur in patients older than 40 years. It predominantly affects males with a 2:1 male-to-female ratio. Etiology Poststreptococcal glomerulonephritis (PSGN) is the most common cause of acute glomerulonephritis. Acute infection with group A beta-hemolytic strep- tococcus (GABHS) usually begins as pharyngitis and then causes a secondary immunological reaction at the glomeruli. PSGN can also occur after a skin infec- tion with GABHS, known as impetigo. Although AGN most commonly develops because of streptococcal infection, it can also arise because of other types of bacterial, viral, fungal, or parasitic infections. AGN can follow infections such as rubella, mumps,
Basement membrane of blood vessel Endothelial cell
Antibodies attacking antigen
Ag
Antigen
Immune complexes are deposited in wall of blood vessel.
FIGURE 22-7. Glomerular damage in glomerulonephritis. The damage to glomerular membranes in glomerulonephritis is caused by antibodies. These antibodies are commonly acti- vated by Streptococcus bacteria. The antibodies combine with antigen and deposit as immune complexes within the kidney that are normally eliminated in the circulation. However, in glomerulonephritis, the immune complexes accumulate and cause inflammation and membrane damage.
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